By Ed Sutton, MD
As anesthesia providers, it’s important that we understand the physiology and pharmacology involved in cardiac assessment and can converse with other medical providers as we consider anesthetic management and patient assessment. Pulmonary Artery/Venous Hypertension has historically been difficult to manage in the acute setting of anesthesia, often complicated by sudden decompensation that doesn’t respond to normal resuscitation efforts and medications. The thin-walled right ventricle is more susceptible to failure with acute or chronic increases in pulmonary vascular afterload. Reductions in right ventricular ejection fraction will result in diminished left ventricle filling and hypotension, as well as inadequate alveolar gas exchange and resultant hypoxia. Hypoxia acutely increases pulmonary pressures, leading to an acute worsening of the situation. As anesthesia providers, we are well trained to manage acute decreases in left ventricular function with inotropes and chronotropes. However, these same medications in the setting of many types of pulmonary hypertension have the potential to increase pulmonary vascular resistance (PVR) worsening right-sided heart failure and hypotension.
The World Health Organization (WHO) classifies pulmonary hypertension into five groups based on underlying causes (e.g., thromboembolic disease, left heart disease, idiopathic, heritable) and conditions. In anesthesia management and treatment, we must consider only two types with two distinct management requirements: precapillary arterial pulmonary hypertension and postcapillary venous pulmonary hypertension. Postcapillary pulmonary hypertension, or pulmonary venous hypertension, is more commonly recognized and treated by anesthesia providers. Postcapillary venous hypertension occurs with increased pressure in the left ventricle and pulmonary veins. Postcapillary hypertension is most commonly caused by reductions in left ventricular function, often due to ischemic heart disease, left-sided valvular heart disease, and severe systemic hypertension. Chronic left-sided heart failure with postcapillary hypertension, with or without reduced ejection fraction (CHFrEF, CHFpEF), is treated by fluid restrictions and afterload reductions. In acute postcapillary hypertension, an increasing number of anesthesia providers are relying on point-of-care ultrasound data (POCUS) to guide and manage inotropic drugs and fluid therapy. Pulmonary artery catheters (Swan-Ganz), once the gold standard for therapy guidance in complex cases, are increasingly being replaced in the operating room by transesophageal echocardiography (TEE).
Precapillary pulmonary hypertension, regardless of the etiology, can rapidly lead to hemodynamic instability that is refractory to normal resuscitation medications, leading to right-sided heart failure. Remember that oxygen is a direct pulmonary dilator and always needs to be your first line of therapy. Precapillary pulmonary hypertension has several etiologies (e.g., thromboembolic, congenital heart disease, connective tissue disorders), many of which are idiopathic and progressive, often leading to a need for lung transplantation. Management is much more complex than postcapillary pulmonary hypertension, often involving Endothelin receptors, Prostacyclin receptors, and Nitric oxide receptors. IV Epoprostenol, IV and inhaled milrinone, and nitric oxide are used for severe cases with hemodynamic instability but may take hours to arrange and are not usually immediately available for use in noncardiac operating rooms. Chronic stable patients can be treated with phosphodiesterase-5 inhibitors (Viagra, Cialis), which are designed to increase nitric oxide as a potent pulmonary vasodilator. Non intubated unstable patients can be treated with nitroglycerin by jet nebulization, which is converted to nitric oxide. The treatment involves 2mg of NTG (five 0.4mg tablets) placed in 3cc of normal saline and administered by a simple asthma nebulizer.
Patients with moderate to severe precapillary pulmonary hypertension should not be considered candidates for outpatient procedures involving anesthesia. Hypoxia and hypercarbia can acutely worsen symptoms and instability, leading to refractory right-sided heart failure. Management of right-sided heart failure and acute increases in pulmonary pressures with hemodynamic derangements are complex and beyond the scope of ambulatory surgical centers.
